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Trimethylamine N-oxide in atherogenesis: impairing endothelial self-repair capacity and enhancing monocyte adhesion
Open accessAbstract
Several studies have reported a strong association between high plasma level of trimethylamine N-oxide (TMAO) and atherosclerosis development. However, the exact mechanism underlying this correlation is unknown. In the present study, we try to explore the impact of TMAO on endothelial dysfunction. After TMAO treatment, human umbilical vein endothelial cells (HUVECs) showed significant impairment in cellular proliferation and HUVECs-extracellular matrix (ECM) adhesion compared with control. Likewise, TMAO markedly suppressed HUVECs migration in transwell migration assay and wound healing assay. In addition, we found TMAO up-regulated vascular cell adhesion molecule-1 (VCAM-1) expression, promoted monocyte adherence, activated protein kinase C (PKC) and p-NF-κB. Interestingly, TMAO-stimulated VCAM-1 expression and monocyte adherence were diminished by PKC inhibitor. These results demonstrate that TMAO promotes early pathological process of atherosclerosis by accelerating endothelial dysfunction, including decreasing endothelial self-repair and increasing monocyte adhesion. Furthermore, TMAO-induced monocyte adhesion is partly attributable to activation of PKC/NF-κB/VCAM-1.
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“some studies performed on human monocytic THP-1 cells and human umbilical vein endothelial cells (HUVEC) showed that TMAO treatment enhanced monocyte adhesion through the PKC/NF-κB pathway, thus increasing the expression of VCAM-1 [58].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [58]
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Metadata
- Authors
- Ma, G., Pan, B., Chen, Y., Guo, C., Zhao, M., Zheng, L., & Chen, B.
- Affiliations
- Department of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, Beijing 100050, China
- Peking University (CN)
- Capital Medical University (CN)
- Corresponding author
- Zheng, LeMin
- Chen, BuXing
- Venue
- Bioscience Reports
- Publisher
- Portland Press Ltd.
- Published
- 2017-03-02
- Volume
- 37
- Issue
- 2
- ISSN
- 0144-8463 (ISSN-L)
- 1573-4935
- PMC
- PMC5333780
- OpenAlex
- W2583372114
- Cited by
- 267
- References
- 46
- Citations by year
- 2026: 14 · 2025: 35 · 2024: 29 · 2023: 45 · 2022: 36 · 2021: 31 · 2020: 35 · 2019: 18 · 2018: 16 · 2017: 8
- FWCI
- 15.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Bioscience Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Greater South Information System
- Funders
- Academy of Medical Sciences
- National Natural Science Foundation of China (81172500, 81170101, 81570321, 81370235)
- Chinese Academy of Sciences
- Chinese Academy of Medical Sciences
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- trimethylamine N-oxide, atherosclerosis, endothelial dysfunction, monocyte adhesion, VCAM-1, protein kinase C, NF-κB, endothelial cell migration, endothelial cell proliferation, extracellular matrix adhesion, human umbilical vein endothelial cells
- MeSH terms
- Cell Adhesion, Cells, Cultured, Humans, Methylamines, Monocytes, Protein Kinase C, Signal Transduction, NF-kappa B, Vascular Cell Adhesion Molecule-1, Atherosclerosis, Human Umbilical Vein Endothelial Cells
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